We also identified multiple drugs targeting high TMSB10 expression and validated that knockdown of TMSB10 improved the efficacy of selumetinib (a MEK1/2 inhibitor approved by the FDA for the treatment of neurofibromatosis-associated tumors) and anti-PD1 in glioma (Fig. 8), providing a promising strategy for improving targeted combination therapy for glioma patients. This evidence concerns the gene TMSB10 and glioma.